Diversity of Gut Bacteria Tied to Metabolic Health

A lower level of intestinal flora diversity was associated with metabolic dysfunction, but a dietary change may enrich gut microbiota and improve metabolic bioclinical markers, according to two studies.

"The present report provides evidence that studies of alterations in our other genome -- the microbial gut metagenome -- may define subsets of adult individuals with different metabolic risk profiles," they wrote. It may help explain some of the heterogeneity seen with adiposity-related phenotypes, they added, providing clues as to why some obese patients can still be metabolically healthy.

The team conducted DNA analysis on intestinal bacteria from 292 Danish patients, 169 of whom were obese and 123 who were not.

They found that 23% of their population had low "bacterial richness," with an average of 380,000 microbial genes, compared with an average of 640,000 genes in those who had more diverse microbiomes.

Patients with lower gene counts had greater adiposity, insulin resistance, and dyslipidemia and a more pronounced inflammatory phenotype than those with high bacterial richness.

And these patients gained significantly more weight over the previous 9 years, the researchers reported.

In terms of microbial communities, anti-inflammatory species such as Faecalibacterium, Bifidobacterium, and Lactobacillus were associated with high diversity, while inflammatory species such as Bacteroides and Ruminococcus were associated with low diversity.

It's not clear why some patients have fewer and less diverse intestinal bacteria, Pedersen and colleagues wrote, but it may have to do with diet, genetic variation, or exposure to antimicrobial agents and other common chemicals such as preservatives and disinfectants.

"We don't know what came first, the chicken or the egg, but one thing is certain: it is a vicious circle that poses a health threat," Pedersen said in a statement.

In a study of 38 obese and 11 overweight patients, Stanislav Dusko Ehrlich, PhD, of the Institut National de la Recherche Agronomique in Jouy en Josas, France, and colleagues found that a 6-week, energy-restricted, high-protein diet plus 6 weeks of weight maintenance led to improvements in the number and diversity of microbial species.

That increase in gene richness was associated with decreases in adiposity, cholesterol, and inflammation, they reported.

But they warned that low baseline gene richness was still associated with greater adipose tissue inflammatory cells at 6 weeks and inflammation at 12 weeks, suggesting that initial gene richness may help predict the effectiveness of dietary interventions in heavier patients.

Still, they concluded, their findings "support a recently reported link between long-term dietary habits and the structure of gut microbiota and suggest that a permanent change of microbiota may be achieved by appropriate diet."

A study in April from Cleveland Clinic researchers found that carnitine -- a substance found abundantly in red meat -- was not directly pro-atherosclerotic, but became a risk for heart disease because of its subsequent interaction with the enzyme TMAO -- which, by the way, was increased in proportion to one's red meat consumption.

In an accompanying editorial to the current two studies, Sungsoon Fang, PhD, and Ronald Evans, PhD, of the Gene Expression Laboratory at the Salk Institute in La Jolla, Calif., said the findings suggest that gut microbial diversity may function as a new biomarker for screening for and treating metabolic disorders.

"Such a concept is promising for clinical research and pharmaceutical drug development, because it opens potential avenues for customizing drugs and reprogramming microbial ecology in individual patients," they wrote.

They cautioned, however, that there is still some debate about using a limited number of enterotypes to classify human gut bacteria, and that the findings also raise the question of whether high microbial gene complexity is "merely a reflection of metabolic health or actually offers protection against disease progression."

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